Infection of IL-4-deficient mice with the parasitic nematode Brugia malayi demonstrates that host resistance is not dependent on a T helper 2-dominated immune response.

Important note: Information in this article was accurate in 1995. The state of the art may have changed since the publication date.

Infection of IL-4-deficient mice with the parasitic nematode Brugia malayi demonstrates that host resistance is not dependent on a T helper 2-dominated immune response.

J Immunol. 1995 Jun 1;154(11):5995-6001. Unique Identifier : AIDSLINE MED/95270994
Lawrence RA; Allen JE; Gregory WF; Kopf M; Maizels RM; Wellcome Research Centre for Parasitic Infections, Department of; Biology, Imperial College of Science, Technology and Medicine,; London, United Kingdom.

Abstract: Resistance of intact mice to infection with the filarial nematode, Brugia malayi is dependent on the presence of T cells. To investigate the role of Th2 cells in this protection, mice with a targeted disruption of the IL-4 gene were infected with different developmental stages of B. malayi. We examined the phenotypic changes in the immune response and the survival of each stage in these mice. In wild-type mice, adult female worms induce Th2 responses, characterized by antigen-specific IgG1 production, elevated IgE, and marked IL-4 secretion by splenocytes stimulated in vitro with Brugia extract. However, first stage larvae (microfilariae), induce Th1 responses with the appearance of antigen-specific IgG2a, IgG2b, and IgG3 and IFN-gamma secretion by splenocytes. Infection of IL-4-deficient mice revealed a dramatic change in the response to adult worms, with a severe reduction in IgG1 production and a corresponding increase in the production of IgG2a, IgG2b, IgG3, and IFN-gamma release. The switch to Th1-type responses was particularly marked in IL-4-deficient recipients of female worms, which continually release live microfilariae. In the absence of IL-4, down-regulation of the microfilarial-induced Th1 response does not occur. Despite these profound alterations to the immune response in IL-4-deficient mice, survival of infective larvae, adult worms, or microfilariae in the peritoneal cavity was unaffected. In mice, therefore, the prominent Th2-type response elicited by filarial parasites may not be an essential component of the host protective immune response.

Keywords: Animal Brugia malayi/*IMMUNOLOGY Enzyme-Linked Immunosorbent Assay Female Filariasis/*IMMUNOLOGY Immunity, Natural/IMMUNOLOGY Immunoglobulins/CLASSIFICATION Interleukin-4/*GENETICS/*IMMUNOLOGY Lymphocyte Transformation Lymphokines/ANALYSIS Male Mice Mice, Knockout Support, Non-U.S. Gov't Th1 Cells/IMMUNOLOGY Th2 Cells/*IMMUNOLOGY JOURNAL ARTICLE
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M9580234

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